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what drug is a selective alpha2 adrenergic receptor agonist?
clonidine
**the alpha2 adrenergic receptor clonidine works where centrally to produce what therapuetic effect?
stimulates alpha2 receptors of inhibitory neurons in the vasomotor center of the medulla in the brainstem; inhibits sympathetic outflow causing a decrease in BP
**in what 2 ways does clonidine produce its affects?
stimulate alpha2 receptors of inhibitoyr neurons in the medulla decreasing sympathetic outflow
inhibts the release of NE peripherally
Plasma catecholamine levels are decreased by up to 50%
6 uses of clonidine besides for hypertension
  • preanesthetic
  • wiht regional to prolong effects of locals
  • diagnose pheochrmoocytoma
  • treat shivering
  • protect against perioperative myocardial ischemia
what is the mechanism that causes rebound hypertension when clonidine is abruptly stopped?
there is an increase in circulating catecholamines wiht increased SVR resulting
3 side effects of clonidine
sedation
bradycardia
dry mouth
what 3 hormones are involved in rebound hypertension from abrupt withdrawal of clonidine





catecholamines
renin
angiotensin II
how should life threatening hypertension associated with clonidine wihtdarwad be treated
reinstitue clonidine therapy or hydralazine or nitroprusside
beta blockers should not be given unless alpha adrenergic blockade is already present
should beta blockers be given to a pt withdrawing from clonidine?
No, b.c beta blockade might exaggerate the magnitude of rebound hypertension by blocking beta2 vasodilating effects.

also, can lead to hrt failure if there is beta blockade and unopposed alpha vasoconstriciton
what drugs can exaggerate the rebound hypertension seen iwht clonidine withdrawal
  • beta blockers
  • tricyclic depressants (potentiate norepinephrine)
ohter than rebound hypertension with sudden withdrawal, wht is th eother anesthetic concner with pt on chronic clonidine?
clonidine can promote perioperative hypothermia
what is the purpose of preoperative clonidine
blunt sympathetic response to laryngoscopy and decrease volatile requirements (↓MAC by 50%)
name 4vasodilators tha tdecrease BP by direct effects on vascular smooth muscle independent of alpha or beta recetpors
  • hydralazine
  • nitroglycerine
  • nitroprusside
  • diazoxide
on what segments of the vascular tree does nitroprusside work to decrease BP
causes venodilation and arterial dilation
4 contraindication for using nitroprusside?
  • liver disease
  • kidney disease
  • hypothyroidism
  • vit B12 deficiency
HOw is cyanide produced?
the ferrous iron of nitroprusside reacts with sulfhydryl groups in RBCs and releases cyanide
nitroprusside contains 3 cyanide ions, what 3 reactions may cyanide ions undergo?
  • reacts with methemoglobin
  • reacts with thiosulfate in liver to produce thiocyanide
  • binds to cytochrome oxidase in the tissues, which interfers with normal O2 utilization
**How do cyanide ions interfere with O2 utilization at tissue cytochrome oxidase?
by binding to the oxidase, they uncouple oxidative phosphorylation, preventing ATP formation
**4 hallmark signs of cyanide toxicity
  • metabolic acidosis
  • cardiac arrythmias
  • increase venous O2 content
  • tachyphylaxis
what is the best indicator of cyanide toxicity?
base defecit
arterial blood gses can most accurately assess cyanide toxicity
how do you know when tachyphylaxis has occured with nitroprusside?
when the pt is resistant to hypotensive effects despite increasing infusion to 10mcg/kg/min (range 0.3-10 max dose) for longer than 10 minutes; suspect cyanide toxicity
**the pt is being given nitroprusside drip with ABG: pH7.21, PCO2 32, PO2 104, base excess=-10
what should you do?
turn off nitroprusside
metabolic acidosis due to base excess -10 (base defecit = 10)
during a deliberate hypotensive technique, you have maintained a MAP = 55 wiht nitroprusside.  The MAP begins to increase and continues to increase despite increase the nitroprusside.  what is happening what do you do?
tachyphylaxis
D/C nitroprusside na dgive 100% O2 (possible cyanide toxicity)
what is treatemnt for cyanide toxicity?
sodium thiosulfate (150 mg/kg IV) over 15 minutes. converts cyanide to thiocyanate
how do you treat cyanide toxicity if sodium thiosulfate does not work?
sodium nitrate: converts hemoglobin to methemoglobin, which will  then bind ot cyanide to make cyanomethemoglobin
Vit B12 (hydroxocoblamin)will also bind ot cyanide
When nitroprusside is stared, the PO2 falls.  why?
it inhibits hypoxic pulmonary vasoconstriction, so shunt will increase and V:Q mismatch will increase and decrease PO2
where in the vascular tree does nitroglycerin work and can it casue cyanide toxicity?
primarily in venules and no cyanide toxicity
the therapeutic benefit of nitroglycerin in the treatment of myocardial ischemia is attributed to what?
decreased myocardial workload and thus decreased O2 consumption (due to decreased preload, SV, and BP)
where in the cardiovascular tree does diazoxide work?
(Hyperstat) dilates arterials mostly (decreased afterload)
used to treat hypertensive emergencies, but cannot be titrated to desired BP like nitroprusside can
how does hydralaxine work?
direct vasodilation of arterioles more than veins by:
  • interfering wiht calcium utilization
  • activates quanylyl cyclase to produce cGMP
  • hyperpolarization of smooth muscles via K channels
what syndrome occurs in some pt treated chronically with hydralazine
systemic lupus eryhtematosus-like syndrome in pt on it for >6 months
which of the following antihypertensives can cause angina: NTG, nitroprusside, hydralazine
all
hydralazine: due to reflex increase HR (bad for pt with CAD)
NTG:if diastolic BP fall excessively resulting in decreased coronary perfusion
Nitroprusside: Coronary steal syndrome
whihc antidysrhythmicas are appropriate for treating PVCs?  what is the drug of choice in treating ventricular dysrhythmias?
lidocaine, procanimide, tocainide, flecainide, propafenone, and quinidine
Drug of choice: lidocaine
lidocaine works on what specific tissues of the heart?
ventricular cells, his-Purkinje system
delays the rate of spontaneous phase 4 depolarization
verapmil and diltiazem slow heart rate by working on what phase of the SA node action potential?
slows phase 4 depolarization
slow heart rate = phase 4 of nodal action potential
calcium channel blockers such as verapmil, work on what phase of the ventricular action potential
Phase 2: decrease contractility by blocking entry of calcium during phase 2
on what tissue of the heart does verapmil work: atrial muscle, ventricular muscle, nodal tissue, purkinje network?
for therapuetic effect, it works on nodal tissue (slow HR by slowing phase 4 of action potential)
secondarily works on ventricular tissue (phase 2 of action potential: decrease contractility)
what is the typical cause of postop tachycardia?
usually due to increased SNS influence
usuallly treated by resolving underlying cause (pain, anxiety, full bladder, fluid) or give beta blocker is unresolved
5 drugs or treatments for cardiac dysrhythmias due to digoxin toxicity
  • lidocaine
  • procainamide
  • phenytoin
  • propanolol
  • DC countershock
what drug is particularly useful in treating cardiac ventricular arrythmias ass. with digitalis toxicity?
phenytoin (0.5-1.5 mg/kg) over 5 minutes
which class of antidysrhythmics have local anesthetic properties?
All Class I drugs, however, only lidocaine is used as both local anesthetic and antidysrhythmic
**what is the concnern when giving phenytoin to the hyperglycemic pt?
partially inhibits insulin release and can further incresae bl sugar
what 2 drugs may be used to treat heart block
Atropine or Isoperetonol
describe metabolismm and elimination of adensosine
rapid Enzymatic clearance (less than one minute)
deaminted in plasma or endothelial cells to inosine or adenosine monophosphate (by phosphorylation)
would administrationof adenosine via the ETT be effective?
No, it would be metabolized prior to reaching the heart.  should be administerd into a central line or the right atrium
shoud you treat afib that develops intraoperatively
only treat if it is adversely affecting CV function (hypotension or ventricular tachycardia)
first line treatment: Verapmil (slows coduction through AV node
Esmolol, amiodarone, digitalis, prpanolol can also be used to treat ventricular tachycardia
should digitalis or propanolol be stopped prior to surgery?
no
*should avoid succs, quinidine, beta agonists, and IV calcium in pt on digitalis
what is an adverse side effect of inamrinone that is not seen with milrinone?
thrombocytopenia
what are the CV actions of glucagon?
increases contractiltiy by increasing levels of cAMP
why shoud hyperventilation be avoided inthe pt on digoxin?
b/c hyperventilation may cause hypokalemia, and this can lead to digitalis toxicity
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